Starvation ketoacidosis


  • Etiology: prolonged fasting, eating disorders, severely calorie-restricted diets, restricted access to food
  • Low insulin/high glucagon in fasting state leads to increased lipolysis. Fatty acids initially converted to acety-CoA, which is then oxidized by the Kreb cycle.
  • When Kreb's cycle oversaturated by excessive adipose breakdown, acetyl-CoA enters ketogenic pathway, resulting in ketone body production
  • Mild ketosis (1mmol/L) occurs after fasting for ~12 to 14 hours.
  • Ketoacidosis rises with continued fasting, peaks after 20 to 30 days (8-10mmol/L).

Clinical Features

Differential Diagnosis


  • Serum chemistry (elevated anion gap)
  • VBG
  • Glucose (usually euglycemic or hypoglycemic)
  • Urinalysis (ketonuria)
  • Serum beta-hydroxybutyrate
  • Lactate
  • Salicylate level (if overdose suspected)
  • Serum osmolality (if toxic alcohol ingestion suspected)


  • Dextrose
    • Resultant increased insulin/decreased glucagon secretion to halt ketone production and facilitate ketone metabolism
    • Correct hypokalemia PRIOR to glucose administration (insulin stimulated by dextrose will drive K+ into cells and worsen hypokalemia)
  • Volume resuscitation with Normal saline or lactated ringers
  • Correct any concomitant electrolyte abnormalities
  • Consider risk of refeeding syndrome


  • If mild, can be discharged after correction of acidosis, electrolytes, and hypovolemia
  • If severe, admit

See Also

External Links